Erwinia carotovora subsp. carotovora Pectic Enzymes: In Planta Gene Activation and Roles in Soft-Rot Pathogenesis. Z. Yang. Laboratory for Molecular Biology of Plant Stress, Department of Plant Pathology, Physiology, and Weed Science, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061-0330 U.S.A. C. L. Cramer, and G. H. Lacy. Laboratory for Molecular Biology of Plant Stress, Department of Plant Pathology, Physiology, and Weed Science, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061-0330 U.S.A. MPMI 5:104-112. Accepted 10 September 1991. This article is in the public domain and not copyrightable. It may be freely reprinted with customary crediting of the source. The American Phytopathological Society, 1992.

Pectic enzyme expression in Erwinia carotovora subsp. carotovora was studied on potato tuber slices using a membrane-separated system. Accumulation of mRNAs was sequential for exo-pectate lyase (exo-PL), endo-PL, and endo-polygalacturonase, respectively, and reached maxima by 6-12 hr. Induction kinetics in vitro with polygalacturonic acid differed from in planta kinetics. Accumulations of mRNA were correlated with rotting; under conditions incompatible with pathogenesis, induction was reduced, and exo-PL expression was delayed. Healed slices were resistant to rotting, but challenging E. c. subsp. carotovora were activated for transient endo-PL expression. This suggests that enzyme induction involves cell wall degradation products. Pretreatment of slices with Escherichia coli expressing E. c. subsp. carotovora exo-PL increased in planta accumulation of mRNAs for all three pectic enzymes in E. c. subsp. carotovora applied as a subsequent challenge, indicating that exo-PL reaction products activate other pectic enzyme genes. Endo-PL, expressed from E. coli, induced host accumulation of mRNAs for phenylalanine ammonia-lyase, a marker for plant defense-responses. These results support the hypothesis that pectic enzymes affect virulence by regulating pectic enzyme levels and affect host responses by inducing defense genes.